Effect of Low-Density Lipoprotein Apheresis on Restenosis after Coronary Angioplasty

为明确低密度脂蛋白(LDL)在PTCA前、后即刻是否能有效预防PTCA后冠状动脉病变的再狭窄，进行了一项前瞻性研究。此外，为了确定脂蛋白(A)[Lp(A)]与凝血纤溶因子之间的关系对PTCA术后3个月再狭窄的影响，在PTCA术前和术后3个月采血。前一天和术后第2天，11例患者接受了低密度脂蛋白的分离。对照组6例行经皮冠状动脉腔内成形术(PTCA)，未行低密度脂蛋白(LDL)分离。血浆纤维蛋白多肽A(FPA)、凝血酶抗凝血酶III复合体(TAT)从10.7×19.5 ng/ml降至2.0×2.2 ng/ml，从13.0×2 2.4 ng/ml降至5.3×6.7 ng/ml，而组织纤溶酶原激活物/抑制物复合体(PAPAL复合体)、α2纤溶酶抑制物-纤溶酶复合体(PPI复合体)、D D二聚体均无明显升高。低密度脂蛋白组冠状动脉病变再狭窄率(26.7%)明显低于对照组(41.7%)。提示低密度脂蛋白分离术可有效预防Lp(A)升高患者的冠状动脉病变再狭窄，其原因是凝血活性降低。

A prospective study was performed to determine whether low-density lipoprotein(LDL) apheresis, then performed only immediately before and after percutaneous transluminalcoronary angioplasty(PTCA), is effective in preventing restenosis of coronary artery lesions following PTCA.Furthermore to determine the influence of between lipoprotqin(a) [Lp(a)] and coagulation-fibrinolysis factors to restenosis 3 months after PTCA, blood samples were taken before and after LDL apheresis. The previous day and 2 days after PTCA, 11 patients underwent LDL apheresis. 6 patients of the control group underwent PTCA but did not underwent LDL apheresis. Lp(a) levels were reduced from 576.4* 80.1 mg/L before apheresis to 172.7*80.1 mg/L after apheresis.Serum fibrinopeptide A(FPA) and thrombin antithrombin III complex(TAT) were reduced from 10.7*19.5 ng/ml to 2.0*2.2 ng/ml, from 13.0*22.4 ng/ml to 5.3*6.7ng/ml. But tissue-plasminogen activator/inhibitor complex (PAPAl complex), alpha 2 plasmin inhibitor plasmin complex (PPI complex) and D D dimer were not significantly high after apheresis. The rate of restenosis of coronary artery lesion was significantly lower in the LDL apheresis group (26.7%) than in the control group (41.7%). These findings suggest that LDL apheresis is effective in preventing restenosis of coronary artery lesions in patients with high plasma Lp(a) because reduction of coagulationactivity.